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Dr. Pickart asked me to post this to the forums. Please read and enjoy. Got questions about this musing? Ask and Dr. Pickart will answer it.

This information is for the use of medical researchers and persons interested in health sciences. It must be emphasized that GHK and other copper binding peptides have not been tested and approved for the treatment of human diseases.

The primary cause of human aging and its attendant diseases are changes in the activity of the human genome. During aging there is an increase in the activity of inflammatory, cancer promoting, and tissue destructive genes plus a decrease in the activity of regenerative and reparative genes.

Regenerative copper peptides appear to help maintain wellness and youth. The human peptide GHK induces a plethora of health associated actions such as tissue repair, anti-inflammatory actions, anti-cancer effects, anti-infection, stem cell activation, increasing protein P63, and so on. Gene data from the Broad Institute indicates that GHK controls or strongly influences 31.8% of the human genes - increasing the output in 59%, and reducing it in 41%, of the genes.

In 2010, The Broad's Connectivity Map predicted that GHK, at a low and non-toxic level, would reverse the effects of aggressive, metastatic human colon cancer on 38 critical cancer-spreading genes. Specifically, it found that the cancer was suppressing genes used to kill cancer cells; the programmed cell death apoptosis system. Cells have "checkpoints" to determine if DNA is made properly and if it is not, the programmed cell death system terminates the cell. Recently, it was found that GHK did not harm certain normal cells, but acted reset the programmed cell death in human cancer cells and inhibit their growth. GHK-Cancer

In 2012, the Connectivity Map indicated that GHK would shift the gene output in severe emphysema in chronic obstructive lung disease (COPD) and shut down tissue destructive genes while increasing the output of genes associated with tissue healing and remodeling. This prediction was confirmed when tested on cells from patients with the disease where GHK, at a very low and non-toxic level, shifted the cellular genes patterns from tissue destruction to tissue repair. GHK-Emphysema

The Holy Grail of genome research is resetting the genes for health. GHK appears to do this on a wide range of tissues and diseases. Since GHK was originally isolated as a factor high in young persons but that declines with age, it is also possible that the molecule might restore humans to a biologically younger state.

Last edited by skinbiologywebmaster
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I am sure either Jessica or Dr. Pickart will answer this more fully in the future, but supplementing with copper will not increase GHK in our bloodstream. Supplementing copper is great for health benefits (check out our forum about copper and disease.) but does not affect the amount of  GHK Copper in the blood.


Although related, those are two separate things.


What would be needed is a supplement of GHK Copper. This does not exist at the moment. Dr. Pickart would love to have this be a daily supplement. He hopes one  day it will come in the future.

US Department of Agriculture studies found the best biochemical anti-oxidants results in humans were with 5 to 6 mgs of supplemental copper daily.


More copper will help to some extent. The copper transport molecules are only about 50% loaded with copper in humans and more copper will increase their activity.


The Recommended Daily Intake (RDA) of copper is 0.7 mgs daily but this is far too low. A human study found the a group of 24 men on a diet of 1.03 mgs total nutritional copper daily developed health problems in 6 weeks. Four of the men developed serious heart arrhythmias and one suffered a myocardial infarction (heart attack).


Am J Clin Nutr. 1985 Aug;42(2):242-51.

Indices of copper status in humans consuming a typical American diet containing either fructose or starch.


Twenty-four male subjects originally participated in a study to determine the effects of feeding diets comparatively low in copper (1.03 mg/day/2850 kcal) and containing either 20% fructose or starch on indices of copper status. During the course of feeding the diets for 11 wk, four of the subjects exhibited heart-related abnormalities and were removed from the study. Fructose ingestion had no effect on serum ceruloplasmin activity or serum copper concentration but did significantly reduce cuprozinc superoxide dismutase (SOD) activity of erythrocytes as compared to starch. Repletion of the subjects with 3 mg copper/day for 3 wk significantly increased SOD levels in subjects previously fed fructose but not starch. Apparent copper balance was significantly greater when the subjects consumed the fructose as compared to the starch diet. These results suggest that the type of dietary carbohydrate fed can differentially affect indices of copper status in humans.



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